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      The protective role of MiR-206 in regulating cardiomyocytes apoptosis induced by ischemic injury by targeting PTP1B

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          Abstract

          MicroRNAs play essential roles in the regulation and pathophysiology of acute myocardial infarction (AMI). The purpose of the present study was to assess the expression signature of miR-206 in rat heart with AMI and the corresponding molecular mechanism. The expression of miR-206 significantly decreased in the infarcted myocardial areas and in hypoxia-induced cardiomyocytes, compared with that in the noninfarcted areas. Overexpression of miR-206 decreased cardiomyocytes apoptosis and the down-regulation of miR-206 increased cardiomyocytes apoptosis in vitro. In addition, overexpression of miR-206 in rat heart in vivo remarkably reduced myocardial infarct size and cardiomyocytes apoptosis. We identified that miR-206 had a protective effect on cardiomyocytes apoptosis with the association of its target protein tyrosine phosphatase 1B (PTP1B). Gain-of-function of miR-206 inhibited PTP1B expression and loss-of-function of miR-206 up-regulated PTP1B expression. Furthermore, overexpression of PTP1B significantly increased cardiomyocytes apoptosis. These results together suggest the protective effect of miR-206 against cardiomyocytes apoptosis induced by AMI by targeting PTP1B.

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          miR-126 regulates angiogenic signaling and vascular integrity.

          Jason Fish, Massimo M. Santoro, Sarah Morton … (2008)
          Precise regulation of the formation, maintenance, and remodeling of the vasculature is required for normal development, tissue response to injury, and tumor progression. How specific microRNAs intersect with and modulate angiogenic signaling cascades is unknown. Here, we identified microRNAs that were enriched in endothelial cells derived from mouse embryonic stem (ES) cells and in developing mouse embryos. We found that miR-126 regulated the response of endothelial cells to VEGF. Additionally, knockdown of miR-126 in zebrafish resulted in loss of vascular integrity and hemorrhage during embryonic development. miR-126 functioned in part by directly repressing negative regulators of the VEGF pathway, including the Sprouty-related protein SPRED1 and phosphoinositol-3 kinase regulatory subunit 2 (PIK3R2/p85-beta). Increased expression of Spred1 or inhibition of VEGF signaling in zebrafish resulted in defects similar to miR-126 knockdown. These findings illustrate that a single miRNA can regulate vascular integrity and angiogenesis, providing a new target for modulating vascular formation and function.
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            Phylogenetic shadowing and computational identification of human microRNA genes.

            Eugene Berezikov, Victor Guryev, Jose van de Belt … (2005)
            We sequenced 122 miRNAs in 10 primate species to reveal conservation characteristics of miRNA genes. Strong conservation is observed in stems of miRNA hairpins and increased variation in loop sequences. Interestingly, a striking drop in conservation was found for sequences immediately flanking the miRNA hairpins. This characteristic profile was employed to predict novel miRNAs using cross-species comparisons. Nine hundred and seventy-six candidate miRNAs were identified by scanning whole-genome human/mouse and human/rat alignments. Most of the novel candidates are conserved also in other vertebrates (dog, cow, chicken, opossum, zebrafish). Northern blot analysis confirmed the expression of mature miRNAs for 16 out of 69 representative candidates. Additional support for the expression of 179 novel candidates can be found in public databases, their presence in gene clusters, and literature that appeared after these predictions were made. Taken together, these results suggest the presence of significantly higher numbers of miRNAs in the human genome than previously estimated.
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              MicroRNA expression signature and the role of microRNA-21 in the early phase of acute myocardial infarction.

              Xiaojun Liu, SHIMIN DONG, Chunxiang Zhang … (2009)
              Several recent reports have suggested that microRNAs (miRNAs) might play critical roles in acute myocardial infarction (AMI). However, the miRNA expression signature in the early phase of AMI has not been identified. In this study, the miRNA expression signature was investigated in rat hearts 6 h after AMI. Compared with the expression signature in the noninfarcted areas, 38 miRNAs were differentially expressed in infarcted areas and 33 miRNAs were aberrantly expressed in the border areas. Remarkably, miR-21 expression was significantly down-regulated in infarcted areas, but was up-regulated in border areas. The down-regulation of miR-21 in the infarcted areas was inhibited by ischemic preconditioning, a known cardiac protective method. Overexpression of miR-21 via adenovirus expressing miR-21 (Ad-miR-21) decreased myocardial infarct size by 29% at 24 h and decreased the dimension of left ventricles at 2 weeks after AMI. Using both gain-of-function and loss-of-function approaches in cultured cardiac myocytes, we identified that miR-21 had a protective effect on ischemia-induced cell apoptosis that was associated with its target gene programmed cell death 4 and activator protein 1 pathway. The protective effect of miR-21 against ischemia-induced cardiac myocyte damage was further confirmed in vivo by decreased cell apoptosis in the border and infarcted areas of the infarcted rat hearts after treatment with Ad-miR-21. The results suggest that miRNAs such as miR-21 may play critical roles in the early phase of AMI.
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                Author and article information

                Contributors
                Hongwei Dang:
                ORCID: http://orcid.org/0000-0003-2666-9872
                Xin Zhang
                Journal
                Journal ID (nlm-ta): Biosci Rep
                Journal ID (iso-abbrev): Biosci. Rep
                Journal ID (publisher-id): bsr
                Title: Bioscience Reports
                Publisher: Portland Press Ltd.
                ISSN (Print): 0144-8463
                ISSN (Electronic): 1573-4935
                Publication date Collection: 31 January 2020
                Publication date (Electronic): 17 January 2020
                Volume: 40
                Issue: 1
                Electronic Location Identifier: BSR20191000
                Affiliations
                Department of Cardiology, Central Hospital of Baoji City, Shannxi Province 721008, P.R. China
                Author notes
                Correspondence: Hongwei Dang ( nyrfzmh9961929882@ 123456126.com ) or Xin Zhang ( bejwbg1664947006@ 123456126.com )
                Author information
                http://orcid.org/0000-0003-2666-9872
                Article
                Publisher ID: BSR20191000
                DOI: 10.1042/BSR20191000
                PMC ID: 6970065
                PubMed ID: 31894853
                SO-VID: 014aaabb-943a-4fce-b033-9e1c5fc5c6bc
                Copyright © © 2020 The Author(s).
                License:

                This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY).

                History
                Date received : 14 April 2019
                Date revision received : 03 December 2019
                Date accepted : 17 December 2019
                Date: 02 January 2020
                Page count
                Pages: 10
                Categories
                Subject: Cardiovascular System & Vascular Biology
                Subject: Gene Expression & Regulation
                Subject: Molecular Bases of Health & Disease
                Subject: Research Articles

                ScienceOpen disciplines: Life sciences
                Keywords: acute myocardial infarction,cardiomyocytes apoptosis,mir-206,protein tyrosine phosphatase 1b
                Data availability:
                ScienceOpen disciplines: Life sciences
                Keywords: acute myocardial infarction, cardiomyocytes apoptosis, mir-206, protein tyrosine phosphatase 1b

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